Influence of blood group on the availability of receptors for attachment of uropathogenic Escherichia coli

Abstract

Escherichia coli strains with defined receptor specificity were used as probes to analyze the individual variation in host cell receptors with respect to blood groups. The adhesins were initially characterized as mannose sensitive (MS), mannose resistant (MR), or nonagglutinating (-). The receptor specificity of the strains with MR adhesins was defined by agglutination of synthetic Galkl-4Galp covalently linked via a spacer arm, (CH2)2S(CH2)2CO-H-bovine serum albumin (BSA) to BSA-latex beads as specific for the globoseries glycolipid receptors (MR:GS). Strains with MR adhesins not reacting with Gala1-4Gal0-BSAlatex were designated MR:nonGS. The attachment and hemagglutination of the MR:GS strains was strictly dependent on Galal-*4Galp-containing receptors, as shown by the absence of binding to cells from individuals of blood group P lacking these structures. Previous reports showed differences in the composition of globoseries glycolipids between erythrocytes from individuals of P1 and P2. No significant difference was found, However, in the the mean adhesion to P1 and P2 epithelial cells or in the agglutination titer for P1 and P2 erythrocytes. The MR:GS receptors were equally distributed on squamous and transitional epithelial cells. In contrast, the distribution of MR:nonGS receptors was skewed. Attachment occurred mostly to squamous epithelial cells. The attachment of strains with MR:nonGS adhesins was independent of the P blood group of the cell donor. The binding ability of MR:GS and MR:nonGS adhesins appeared independent and additive. The attachment was not influenced by the ABH blood group. However, increased binding to epithelial cells from nonsecretors occurred regardless of the P blood group, suggesting a shielding of receptors by products controlled by the secretor genes. These results illustrate how individual variation in cell surface components with and without receptor activity determine the interaction of a ligand with a known receptor. Adhesive capacity is a virulence factor for Escherichia coli causing upper urinary tract infection (25). The attachment results from the interaction of host cell receptors with bacterial surface structures known as adhesins (14). Since the exact structures of the adhesins remain to be determined, they are classified according to either target cell specificity or, in some instances, receptor specificity (when the receptor structure has been identified). Wild-type bacteria, e.g., urinary E. coli isolates, can coexpress several adhesins, even on a single bacterial cell (5, 10). Receptors for attaching bacteria can consist of host cell surface carbohydrates, i.e., either glycoproteins or glycolipids (12). Several glycoconjugate specificities have been suggested to mediate adhesion or hemagglutination of uropathogenic E. coli, including mannose (19), N-acetylglucosamine (27), M antigen (28), NeuAca2-3Gal (21), and 919

Effect of host Lewis and ABO blood group antigen expression on Helicobacter pylori colonisation density and the consequent inflammatory response

“…A hypothesis has been suggested that the decreased susceptibility of secretors to peptic ulcer disease is due to the presence of terminal fucose resi-dues of H type 2 and Le being important receptors for H. pylori, and that the presence of these antigenic determinants in the mucosa of secretors, protects them from heavy colonisation by infecting organisms [12]. Previous reports have demonstrated that epithelial cells of non-secretors bind larger numbers of micro-organisms than cells of secretors, speci¢cally, uropathogenic strains of Escherichia coli [15], Candida albicans [16], and Staphylococcus aureus [9].…”

Non-secretion of ABO blood group antigens: a host factor predisposing to recurrent urinary tract infections and renal scarring

“…Small numbers of microorganisms might elicit a modest inflammatory response and induce antibodies specific for the particular strain. Second, in the non-immune non-secretor, colonization might not be inhibited but enhanced by interactions with Lewis a antigens as suggested by studies with candida [22,23] and by increased attachment of uropathogenic strains to cells of nonsecretors [12]. The larger population of bacteria might multiply in the absence of specific immune protection and induce a strong inflammatory response.…”

Moraxella (Branhamella) catarrhalis Adherence to Human Bronchial and Oropharyngeal Cells: The Role of Adherence in Lower Respiratory Tract Infections

“…Bacterial adherence to epithelial cells depends on receptor expression by the host (11,25). Patients with cystic fibrosis were recently shown to have a higher density of receptors for P aeruginosa on their respiratory tract epithelial cells than controls (24).…”